Suppression of TLR2-induced IL-12, reactive oxygen species, and inducible nitric oxide synthase expression by Mycobacterium tuberculosis antigens expressed inside macrophages during the course of infection

J Immunol. 2010 May 15;184(10):5444-55. doi: 10.4049/jimmunol.0903283. Epub 2010 Apr 12.

Abstract

We report the enrichment of and immune responses mediated by genes expressed by Mycobacterium tuberculosis inside macrophages as a function of time. Results indicate that M. tuberculosis expresses different genes at different times postinfection. Genes expressed early (day 1) following infection enhance M. tuberculosis-mediated activation of dendritic cells (DCs), whereas genes expressed later (day 5) in the infection prevent DC activation. However, all genes downmodulated MHC class I and II expression on infected macrophages, thus compromising their ability to interact with Ag-specific T cells. Day-1 and -5 genes downmodulated proinflammatory cytokine production from DCs, thus impairing signal 3 during DC-T cell cognate interactions. Consequently, T cells activated by Ag-experienced DCs secreted low levels of IFN-gamma and IL-17 but maintained high IL-10 secretion, thus inducing suppressor responses. Further characterization revealed that day-1 and -5 genes increased TLR2-induced expression of suppressors of cytokine signaling 1 from DCs and downmodulated IL-12 expression. In addition, day-1 and -5 genes prevented the generation of reactive oxygen species in DCs. In contrast, although day-5 genes increased TLR2-mediated suppressors of cytokine signaling 1 expression in macrophages, day-1 genes downmodulated the expression of inducible NO synthase 2. Similar downregulation of immune responses was observed upon exogenous stimulation with day-1 or -5 Ags. Finally, day-1 and -5 genes promoted enhanced survival of M. tuberculosis inside DCs and macrophages. These results indicate that M. tuberculosis genes, expressed inside infected macrophages as a function of time, collectively suppress protective immune responses by using multiple and complementary mechanisms.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Bacterial / biosynthesis
  • Antigens, Bacterial / genetics
  • Antigens, Bacterial / physiology*
  • Cell Line, Tumor
  • Female
  • Gene Expression Profiling* / methods
  • Humans
  • Immune Tolerance / genetics
  • Interleukin-12 / antagonists & inhibitors*
  • Interleukin-12 / biosynthesis
  • Interleukin-12 / genetics
  • Macrophages / enzymology
  • Macrophages / immunology*
  • Macrophages / microbiology
  • Macrophages, Peritoneal / enzymology
  • Macrophages, Peritoneal / immunology
  • Macrophages, Peritoneal / microbiology
  • Mice
  • Mice, Inbred BALB C
  • Mycobacterium tuberculosis / genetics
  • Mycobacterium tuberculosis / immunology*
  • Nitric Oxide Synthase Type II / antagonists & inhibitors*
  • Nitric Oxide Synthase Type II / biosynthesis
  • Nitric Oxide Synthase Type II / genetics
  • Reactive Oxygen Species / antagonists & inhibitors*
  • Reactive Oxygen Species / metabolism
  • Time Factors
  • Toll-Like Receptor 2 / antagonists & inhibitors
  • Toll-Like Receptor 2 / physiology*
  • Tuberculosis, Pulmonary / enzymology
  • Tuberculosis, Pulmonary / immunology
  • Tuberculosis, Pulmonary / pathology

Substances

  • Antigens, Bacterial
  • Reactive Oxygen Species
  • Tlr2 protein, mouse
  • Toll-Like Receptor 2
  • Interleukin-12
  • Nitric Oxide Synthase Type II